The document summarizes key aspects of the endocrine system. It describes how the endocrine system consists of ductless glands that secrete hormones directly into the bloodstream to regulate distant target cells. The endocrine and nervous systems are both regulatory systems that utilize different mechanisms - the endocrine system provides longer-term control of things like metabolism and development through hormones, while the nervous system provides faster responses. The major glands of the endocrine system and their hormones are also outlined.

1. The Endocrine System
Chapter 17

2. Intercellular Communication
Cell Target Cell
Cell
Cell Target Cell
Target CellNeuron
Hormone
Hormone
Hormone Hormone
Hormone
Hormone
Hormone
Endocrine
Paracrine
Autocrine
Blood
Neuroendocrine
Blood
Interstitial Fluid
Interstitial Fluid

3. The endocrine system consists of the ductless
glands.
• They are not connected
anatomically. These glands
secrete hormones into the blood.
A hormone travels in the blood,
signaling to distant target cells.
• Neurosecretory neurons release
neurohormones. They are also
distributed by the blood to target
cells.
• Target cells are specific for each
hormone or neurohormone. It is
specific, as these cells have
receptors that uniquely bind to a
specific chemical messenger.

4. The endocrine and nervous systems are two regulatory
systems of the body.
• The endocrine system mainly controls activities that require longer
duration. This system has several overall functions.
• It regulates organic metabolism and water/electrolyte balance. It
also induces adaptive changes to deal with stress. The endocrine
system promotes smooth, sequential growth and development.
• Some hormones control reproduction while another one regulates
red blood cell production. Some hormones regulate circulatory and
digestive functions.
• A tropic hormone regulates the secretions of another endocrine
gland. Tropic hormones are secreted by the anterior pituitary
gland.

5. • Peptide & Protein Hormones
• Steroid Hormones
• Amine Hormones
Classes of Hormones

6. Chemical Classification of Hormones
• Amine hormones are derived from tyrosine or tryptophan
• Include NE, Epi, thyroxine, melatonin
• Polypeptide/protein hormones are chains of amino acids
• Include ADH, GH, insulin, oxytocin, glucagon, ACTH,
PTH
• Glycoproteins
• Long polypeptide bound to a carbohydrate group
• Include LH, FSH, TSH, hCG
• Steroids are lipids derived from cholesterol
• Include testosterone, estrogen, progesterone & cortisol
11-7

7. Hypothalamus
Anterior pituitary
Posterior pituitary
Thyroid
Pancreas
Liver
Parathyroid
• TRH, GnRH, CRH
GHRH, Somatostatin,
• ACTH, TSH, FSH, LH,
PRL, GH
• Oxytocin, ADH
• Calcitonin
Insulin,Glucagon,
Somatostatin
Somatomedin C (IGF-1)
• PTH
Placenta
Kidney
Heart
G.I. tract
Adipocyte
• HCG, HCS or HPL
• Renin
ANP
Gastrin, CCK,
Secretin, GIP,
Somatostatin, GLP-1
•Leptin
Gland/Tissue Hormones Gland/Tissue Hormones
Peptide & Protein Hormones

8. Adrenal Cortex
Testes
Ovaries
Corpus Luteum
Placenta
Kidney
• Cortisol, Aldosterone,
Androgens
• Testosterone
• Estrogens, Progesterone
• Estrogens, Progesterone
• Estrogens, Progesterone
• 1,25-Dihydroxycholecalciferol
Gland/Tissue Hormones
Steroid Hormones

9. Amine Hormones
Hypothalamus
Thyroid
Adrenal medulla
• Dopamine
• T3, T4
• NE, EPI
Gland/Tissue Hormones

10. The mechanisms of hormone synthesis, storage,
and secretion vary according to the class of
hormone.
• Peptide hormones have precursors called preprohormones. They
are made on ribosomes of the ER. In the Golgi complex they are
converted to prohormones and, finally, active hormones. The Golgi
complex concentrates these hormone into secretory vesicles.
• These hormones are released from endocrine cells by exocytosis.
• Cholesterol is the common precursor for all steroid hormones. A
series of enzymatic steps modify this molecule into a different
hormone in a specific endocrine cell. Only the precursor
(cholesterol) is stored. The lipid-soluble hormone is not stored.
• The amine hormones are made from tyrosine.

11. All hormones are transported in the blood.
However, they are not transported in the
same way.
• Hydrophilic (water soluble) hormones are dissolved in the plasma.
Most lipophilic (lipid soluble) hormones are bound reversibly to
plasma proteins. These hormones are released by these proteins
when they actively signal target cells.
• Hormones generally produce their effect by altering intracellular
proteins.
• Hydrophilic hormones bind to receptors on the surface of target
cells. Lipophilic hormones pass through target cell membranes and
bind to receptors inside the target cell.
• A few hydrophilic hormones alter the permeability of the target
cell’s membrane.

12. Other effects on hormone activity include:
• The concentration of a hormone in the blood is subject to control. It varies according to
homeostatic need.
• The availability of a hormone to its receptor depends on the hormone’s rate of secretion, its
rate of metabolic activation, the extend of its binding to plasma proteins if it is lipophilic, and
its removal from the blood. Removal can be by metabolic inactivation or urinary excretion.
• Negative feedback maintains the plasma concentration of a hormone at a needed level.
When a hormone’s concentration falls below a certain set point, the gland increases the
secretion of the hormone. When the hormone’s level is above the set point, the secretion
decreases.
• Many endocrine control systems involve neuroendocrine reflexes. Neural input to a gland
regulates the gland’s secretion.
• The secretion rate of many hormones varies by a diurnal or circadian rhythm.

13. Endocrine disorders result from the
hyposecretion or hypersecretion of a
hormone.
• Factors producing hyposecretion include heredity, dietary
deficiency, immunologic factors, and disease processes.
Hyposecretion can be primary or secondary (due to the deficiency
of the hormone’s tropic hormone).
• Replacement therapy of a hormone can often successfully treat the
conditions from hyposecretion.
• Hypersecretion of a hormone can also be primary or secondary.
Factors producing hypersecretion include tumors on the endocrine
gland and immunologic factors.
• Endocrine dysfunction can also arise from the unresponsiveness of
target cells to a hormone.

14. Table 17-1a, p. 533

15. Table 17-1b, p. 534

16. Table 17-1c, p. 534

17. Table 17-1d, p. 535

18. Table 17-1e, p. 535

19. The pituitary gland is a small
structure at the base of the brain.
• The posterior lobe is the neurohypophysis. It is
composed of nervous tissue. The anterior lobe is
the adenohypophysis. It is glandular tissue.
• The posterior lobe and the hypothalamus act as a
unit to secrete vasopressin and oxytocin. The
axons of the hypothalamus pass from the brain into
capillaries in the posterior lobe.
• The posterior lobe does not produce vasopressin
and oxytocin. They are produced by hypothalamic
neurons. They are stored in neuron terminals in
the posterior lobe.
• Vasopressin (ADH) signals the kidneys to retain
water. It also signals the smooth muscle in the
walls of arterioles. Its main role is regulating water
balance.

20. The anterior pituitary secretes six
hormones. Many are tropic.
• By a vascular network with the hypothalamus, each anterior
pituitary hormone is secreted through signaling by a releasing
hormone from this region of the brain.
• The thyroid-stimulating hormone (TSH) stimulates the secretion
and growth of the thyroid gland.
• The adrenocorticotropic hormone (ACTH) stimulates the growth
and secretion of hormones from the adrenal cortex.
• The follicle-stimulating hormone (FSH) stimulates growth and
development of the ovarian follicles in females and sperm
production in males.
• The luteinizing hormone (LH) stimulates ovulation and luteinization
(female) and stimulates testosterone secretion in the male.
• Prolactin enhances breast development in females.

21. Fig. 17-6a, p. 539
Hypothalamus
Anterior pituitary
Posterior pituitary
TSH
Thyroid
gland
Thyroid hormone
(T3 and T4)
Metabolic rate
ACTH
Adrenal
cortex
Cortisol
Metabolic actions;
stress response
Prolactin
Mammary
glands
Breast growth
and milk
secretion

22. Fig. 17-6b, p. 539
Hypothalamus
Anterior pituitary
Posterior pituitary
TSH ACTH
Growth hormone
Liver
Somatomedins
Many tissues
Metabolic
actions
Bone Soft tissues
Growth
or

23. Fig. 17-6c, p. 539
Hypothalamus
Anterior pituitary
Posterior pituitary
TSH ACTH
Growth hormone
LH FSH
Gonads (ovaries in females, testes in males)
Sex hormone secretion
(estrogen and
progesterone in females,
testosterone in males)
Gamete production
(ova in females,
sperm in males)

24. Hypothalamic releasing and inhibiting hormones
regulate anterior pituitary hormone secretion.
• TRH stimulates the release of TSH.
• CRH stimulates the release of ACTH.
• GnRH stimulates the release of FSH and LH.
• GHRH stimulates the release of the growth
hormone.
• GHIH inhibits the release of the growth hormone
and TSH.
• PRH stimulates the release of prolactin.
• PIH inhibits the release of prolactin.
• A hypothalamic hormone controls the output of an
anterior pituitary hormone. The tropic hormone
regulates the secretion of the target endocrine
gland’s hormone.

25. Table 17-2, p. 540

26. The hypothalamic regulatory hormones
reach the anterior pituitary by a vascular
link.
• This is a capillary to capillary connection, the hypothalamic-
hypophyseal portal system. Blood is this system carries
hypothalamic signals to the anterior pituitary.
• Regulation of the secretion of the hypothalamic hormones depends
on numerous inputs. Their complete regulation is not well
understood.
• Target gland hormones inhibit hypothalamic and anterior pituitary
hormone secretion via negative feedback.
• For example, a rise in cortisol from the adrenal cortex can feed
back and reduce CRH secretion (hypothalamus) and the sensitivity
of the ACTH secreting cells (anterior pituitary) to CRH.
• If cortisol falls in the blood, the direction of the other responses is
reversed.

27. Fig. 17-8, p. 541
Hypothalamus
Anterior pituitary
Posterior pituitary
Neurosecretory
neurons
Systemic arterial inflow
Hypothalamic-hypophyseal
portal system
System
venous
outflow
= Hypophysiotropic Hormones = Anterior pituitary hormone

28. The endocrine system controls growth.
• Growth is signaled by the growth hormone. There are other factors that
influence growth.
• Growth capacity is genetically determined. Adequate diet, freedom from
chronic disease and stress, and normal levels of other growth-influencing
hormones are other factors.
• The growth hormone does not play a role in fetal development. In children
there is a postnatal growth spurt. The growth hormone may play a role in
the later-occurring pubertal growth spurt. Androgens also contribute at this
time.

29. The growth hormone has metabolic
effects.
• It mobilizes fat stores (lipolytic) as a major
energy source while conserving glucose for
glucose-dependent tissues. This metabolic
action is unrelated to growth.
• The growth hormone promotes growth by
signaling an increase in the number of cells and
size of cells in target organs. It stimulates the
uptake of amino acids and protein synthesis in
target cells.
• The growth hormone stimulates growth in the
length and thickness of long bones.
• It stimulates the lengthening of bones at the
epiphyseal plate. It stimulates osteoblast
activity and the proliferation of epiphyseal
cartilage. New bone tissue replaces cartilage in
this region.
• It stimulates bone thickness by activating
osteoblasts under the periosteum.

30. Fig. 17-6b, p. 539
Hypothalamus
Anterior pituitary
Posterior pituitary
TSH ACTH
Growth hormone
Liver
Somatomedins
Many tissues
Metabolic
actions
Bone Soft tissues
Growth
or

31. The growth hormone exerts its effects indirectly by stimulating
somatomedins.
• These substances are also called insulin-like
growth factors. They are stimulated by the
growth hormone and mediate most of the
growth-promoting effects of the hormone.
• The main source of these factors is the liver.
Their production depends on adequate
nutrition. Their production is also related to
age.
• The secretion of the growth hormone is
regulated by GHRH and GHIH.
• Many factors influence the secretion of the
growth hormone. It increases one hour after a
deep sleep. Exercise can increase the
secretion of the growth hormone. An
abundance of amino acids and hypoglycemia
increase its release.

32. Fig. 17-10, p. 545
Exercise, stress,
blood glucose
Blood amino acids,
Blood fatty acids
Hypothalamus
Diurnal
rhythm
Growth hormone–
releasing hormone
(GHRH)
Growth hormone–
inhibiting hormone
(GHIH)
Anterior pituitary
Growth hormone
Liver
Somatomedins
Metabolic actions
unrelated to growth:
fat breakdown
( blood fatty acids)
glucose uptake by
muscles
( blood glucose)
Growth-promoting actions:
cell division
protein synthesis
( blood amino acids)
bone growth

33. A deficiency or excess of the growth hormone changes growth
patterns.
• A hyposecretion produces dwarfism in a child. In Laron dwarfism, tissues
fail to respond to the growth hormone.
• In adults a growth hormone deficiency reduces muscle mass and strength.
• A hypersecretion of the growth hormone produces gigantism in the child.
• If hypersecretion occurs after the epiphyseal plates have closed,
acromegaly develops. Only certain bones are affected.
• Other hormones in addition to the growth hormone are essential for normal
growth. The thyroid hormone is essential for growth. Insulin is a growth
promoter. Androgens play a role in a pubertal growth spurt.

34. The pineal gland is a small structure in
the brain.
• It secretes the hormone melatonin. It helps keep the body’s circadian
rhythms in synchrony with the light-dark cycle.
• The suprachiasmatic nucleus (SCN) has a major role in establishing many
of the body’s daily rhythms.
• It secretes clock proteins. Cyclic changes in their concentration changes
the neural output from the SCN.
• The SCN works in conjunction with the pineal gland and pineal gland to
regulate circadian rhythms.
• Daily changes in light intensity is the major environmental factor used to
adjust the SCN master clock.
• Melatonin has other functions not related to circadian timekeeping. It
accomplishes natural sleep without hypnosis (side effects). It inhibits
hormones that stimulate reproductive activity. It is also an effective
antioxidant.

35. The thyroid gland consists of two
lobes of endocrine tissue.
• It lies over the trachea, below the larynx.
• Its follicular cells store colloid. Thyroglobulin
(TGB) is the main constituent of this colloid.
The follicular cells produce two hormones, T4
and T3. These two hormones are collectively
the thyroid hormone. It regulates overall
basal metabolic rate.
• C cells between the follicular cells secrete
calcitonin. It plays a role in calcium
metabolism.
• Tyrosine and iodine are the ingredients for the
thyroid hormone. The thyroid hormone
synthesis occurs on the thyroglobulin
molecules in the colloid.

36. Fig. 17-14, p. 549
Blood
Thyroid follicular cell
*Endoplasmic
reticulum/Golgi
complex
Colloid
TGB = Thyroglobulin
I = Iodine
MIT = Monoiodotyrosine
DIT = Di-iodotyrosine
T3 = Tri-iodothyronine
T4 = Tetraiodothyronine (thyroxine)
Lysosome

37. Thyroid hormone synthesis and storage
occurs through a series of steps.
• Tyrosine is incorporated into TGB. This is transported into the colloid by
exocytosis. Iodine is transported into the colloid by follicular cells.
• The attachment of one iodine to tyrosine produces MIT.
• The attachment of two iodines to tyrosine produces DIT.
• The coupling of two DITs produces T4.
• The coupling of one MIT to two DITS produces T3.
• Thyroid follicular cells engulf a part of TGB-containing colloid by
phagocytosis.
• Lysosomes attack the engulfed vesicle and split the iodinated products
from TGB.
• T4 and T3 reach the blood by diffusion.
• The deiodination of T4 and T3 free the iodine for recycling.
• The thyroid hormone is highly lipophilic. It binds to several plasma
proteins.

38. Most of the T4 is converted to T3 outside the
thyroid. The thyroid hormone has many metabolic
effects.
• T4 loses one of it iodines in the liver or kidney.
• The hormone increases the body’s overall basal metabolic effect. It
regulates the body’s use of oxygen and is calorigenic (heat-
producing).
• Large amounts of the secreted hormone convert glycogen into
glucose and stimulates protein degradation.
• This hormone also has sympathomimetic effects, increasing target
cells’ responsiveness to epinephrine and norepinephrine.
• It increases heart rate and the force of heart contraction.
• It also stimulates growth hormone secretion and promotes the
effect of this hormone on increased protein synthesis.

39. Fig. 17-15, p. 551
Stress Cold in
infants
Hypothalamus
Thyrotropin-
releasing
hormone (TRH)
Anterior pituitary
Thyroid-stimulating
hormone (TSH)
Thyroid gland
Thyroid hormone
(T3 and T4)
Metabolic rate and heat production;
enhancement of growth and CNS
development; enhancement of
sympathetic activity

40. The secretion of the thyroid hormone is
regulated by the hypothalamus-pituitary-
thyroid axis.
• TSH from the anterior pituitary stimulates the release of the
thyroid hormone. TSH also maintains the structural integrity
of the thyroid gland.
• TRH from the hypothalamus turns on TSH secretion. An
increase in the thyroid hormone feeds back to decrease TSH
secretion (negative feedback).
• TRH secretion is increased only by exposure to the cold in
newborn infants.

41. Imbalances in the thyroid hormone cause
changes in development.
• Hypothyroidism produces myxedema in the adult. From birth a
deficiency of the hormone produces cretinism. Causes of these
conditions include deficiency of TRH, TSH, or the thyroid
hormone. A deficiency of iodine in the diet can also be a cause.
• Symptoms include a lowered basal metabolic rate, excessive
weight gain, bradycardia, cold intolerance and the quick onset of
fatigue.
• Grave’s disease is the most common cause of hyperthyroidism. It
is an autoimmune disease. Symptoms include an elevated
metabolic rate, high heart rate, heat intolerance and
exophthalmos.
• A goiter develops when the thyroid gland is overstimulated.
Hypothyroidism leads to high levels of TSH due to only a small
amount of negative feedback. TSH acts on the follicular cells to
increase their size and number.
• A goiter can develop in Grave’s disease due to an increase in
thyroid-stimulating immunoglobulin (TSI).

42. Fig. 17-16, p. 551
Thyroid-stimulating
immunoglobulin (TSI)
Anterior pituitary
No TSH
(No stimulation)
Thyroid gland
Thyroid hormone

43. There are two adrenal glands.
• Each is embedded in a capsule of fat on top of each kidney.
• The outer adrenal cortex of each gland secretes several steroid
hormones. The inner adrenal medulla of each gland secretes
epinephrine and norepinephrine.
• The adrenal cortex consists of three different zones. Each secretes a
different family of hormones.
• One of these zones secretes the mineralocorticoids. The
mineralocorticoids (e.g., aldosterone) signal the kidneys (distal tubule and
collecting duct) to retain sodium (plus water) and eliminate potassium.
Aldosterone secretion is increased by activation of the renin-angiotensin-
aldosterone system.

44. Fig. 17-20, p. 555
Stress Diurnal
rhythm
Hypothalamus
Corticotropin-releasing
hormone (CRH)
Anterior pituitary
Adrenocorticotropic
hormone (ACTH)
Adrenal cortex
Cortisol
Blood glucose
(by stimulating gluconeogenesis
and inhibiting glucose uptake)
Blood amino acids
(by stimulating protein degradation)
Blood fatty acids
(by stimulating lipolysis)
Metabolic fuels
and building blocks
available to help
resist stress

45. One of the zones in the adrenal cortex
secretes the glucocorticoids.
• The glucocorticoids (mainly cortisol) stimulate gluconeogenesis.
This is the conversion of amino acids into carbohydrates, occurring
mainly in the liver.
• Cortisol also facilitates the inhibition of glucose uptake, stimulates
protein degradation, and promotes lipolysis.
• Cortisol plays a major role in the adaptation to stress.
• Noxious stimuli that can produce this include physical, chemical,
physiologic, psychological, emotional, and social sources. An
increased concentration of glucose in the blood is major response
to all of these.
• Pharmacologic levels of cortisol can have anti-inflammatory and
immunosuppressive effects. This can be used to treat rheumatoid
arthritis or allergies. Long-term use of this treatment can produce
unwanted side effects.

46. The secretion of cortisol is regulated by the
hypothalamus-pituitary-adrenal cortex axis.
• ACTH from the anterior pituitary stimulates the
secretion of cortisol from the adrenal cortex.
ACTH secretion is triggered by CRH from the
hypothalamus.
• Negative feedback from cortisol in the blood to
the hypothalamus and the anterior pituitary
regulate the level of cortisol in the blood.
• Increased output of CRH and ACTH increases
in response to stress.
• Cortisol secretion also varies by a diurnal
rhythm.

47. A third zone in the adrenal cortex
secretes androgens or estrogens.
• Both are produced in either sex.
• Usually they are not abundant enough to be powerful in
either sex. The androgens have masculinizing effects.
• The androgen DHEA can have an effect in females who
otherwise lack androgens.
• ACTH controls adrenal androgen secretion.

48. The adrenal cortex may secrete too much or too
little of its hormones.
• Primary hyperaldosteronism is Conn’s syndrome.
• The secondary hyperaldosteronism is due to the high activity of the
renin-angiotensin mechanism.
• Excessive cortisol secretion (Cushing’s syndrome) can be due to
increased amounts of CRH or ACTH, adrenal tumors, or ACTH-
secreting tumors. The main symptom of this condition is excessive
gluconeogenesis.
• Adrenal androgen hypersecretion produces adrenogenital syndrome. It
manifests with different effects depending of the biological sex and age
of the subject.
• Primary adrenocortical insufficiency is known as Addison’s disease.
This is usually an autoimmune disease. The secondary cause of this
insufficiency occurs because of an abnormality of the pituitary or
hypothalamus.
• Symptoms of Addison’s disease include: hypotension, hypoglycemia,
potassium retention and sodium depletion. There is poor response of
the subject to stress and hypoglycemia.

49. The adrenal medulla is the inner core of the
adrenal gland.
• It is signaled by a preganglionic neuron and is a modified postganglionic
neuron. It stores and secretes epinephrine and norepinephrine. They are
released into the blood by sympathetic stimulation.
• These two hormones vary in their affinities for different kinds of alpha and
beta adrenergic receptors on target organs. Epinephrine shows exclusive
beta-2 receptor activation.
• Epinephrine reinforces the sympathetic nervous system and exerts
additional metabolic effects.
• Its responses are the fight or flight responses. This hormone constricts
most blood vessels supplying organs, raising the total peripheral
resistance. However, it dilates the blood vessels supplying the heart and
skeletal muscles.
• Metabolically it promotes glycogenolysis (liver and skeletal muscles) while
stimulating glucagon secretion and inhibiting insulin secretion. This
hormone also promotes lipolysis. It also causes CNS arousal.

50. The stress response is a pattern of reactions to a situation that threatens
homeostasis.
• It is a common group of responses (general adaptation syndrome)
to noxious stimuli. The sympathetic nervous system and
epinephrine have a role in these responses.
• Cardiac output increases. Blood is shunted to the heart and
skeletal muscles while being diverted away from other organs.
• The CRH-ACTH-cortisol system is also activated in these
responses. Glucose is elevated in the blood.
• Blood glucose is elevated by decreased insulin and increased
glucagon secretions.
• The renin-angiotensin-aldosterone system and vasopressin activity
maintain blood pressure and blood volume.
• The multifaceted stress response is coordinated by the
hypothalamus. It activates the sympathetic nervous system and
CRH-ACTH-cortisol release.
• Activation of this response by chronic psychosocial stressors may
be harmful.

51. Fig. 17-23, p. 560
Stressor
Hypothalamus
Sympathetic
nervous
system
CRH
Anterior
pituitary
ACTH
Adrenal cortex
Cortisol
Posterior
pituitary
Vasopressin
Adrenal medulla
Epinephrine
Glucagon-secreting cells
Insulin-secreting cells
Endocrine
pancreas
Glucagon Insulin
Arteriolar
smooth muscle
Vasoconstriction
Blood flow
through kidneys
Renin Angiotensin Aldosterone

52. Table 17-3, p. 559

53. The endocrine system controls fuel metabolism.
• Metabolism is all of the chemical reactions within the cells of the
body. These reactions include the degradation, synthesis, and
transformation of proteins, carbohydrates, and lipids.
• Anabolism is the synthesis of larger organic molecules. Anabolic
reactions require ATP. Catabolism is the breakdown of large
molecules. These reactions can include hydrolysis and the
oxidation of glucose to make ATP.
• Normally the rates of anabolism and catabolism are in balance in
the adult.
• Nutrients from meals must be stored and released between meals.
The brain needs a constant supply of glucose. It cannot store
glycogen.

54. Table 17-4, p. 561

55. Fig. 17-24, p. 562
Food intake
Absorbable units
Dietary protein Dietary
carbohydrate
Dietary triglyceride
fat
D I G E S T I O N
Amino
acids Glucose Fatty
acids Monoglycerides
A B S O R P T I O N
Metabolic pool
in body
Body proteins
(structural or
secretory
products)
Amino
acids
Urea Urinary excretion
(elimination from body)
Storage, structural, and
functional
macromolecules in cells
Glycogen storage
in liver and
muscle
Triglycerides
in adipose tissue
stores (fat)
Glucose
Fatty
acids
Oxidation to
CO2 + H2O + ATP (energy)
Expired
(elimination from body)
Use as metabolic fuel
in cells

56. Nutrients are stored for use between meals.
• Excess circulating glucose is stored as glycogen in the liver and
skeletal muscles.
• Excess circulating fatty acids from the diet are stored into
triglycerides, mainly in adipose tissue.
• Excess amino acids not needed for protein synthesis are converted
to glucose and fatty acids and are ultimately stored as triglycerides
in adipose tissue. Muscles are the main site of amino acid storage.
• During fasting many body cells will burn fatty acids to spare
glucose for the brain. To supply the brain, amino acids can be
converted to glucose by gluconeogenesis.
• Metabolic fuels are stored during the absorptive state. This occurs
when ingested nutrients are being absorbed into the blood.
• Metabolic fuels are mobilized during the postabsorptive state.
Nutrients are not being absorbed at this time. Stored molecules
are catabolized to maintain needed blood concentrations.

57. Table 17-5, p. 563

58. Insulin and glucagon from the pancreas regulate fuel
metabolism.
• They are the dominant hormonal regulators that change metabolic
pathways.
• The endocrine cells in the pancreas are organized into the islets of
Langerhans. The beta cells produce insulin. The alpha cells
produce glucagon. Somatostatin from pancreatic D cells can inhibit
both of these hormones.
• Insulin lowers blood glucose, fatty acid, and amino acid levels. It
promotes their storage.
• Insulin facilitates glucose transport into most cells. A glucose
transporter acts as a plasma membrane carrier to accomplish this
process. Insulin and this transporter also assist the transport of
fatty acids into tissues. Insulin catalyzes the conversion of fatty
acids into glucose.
• Insulin stimulates glycogenesis in skeletal muscle and liver cells.
This hormone inhibits glycogenolysis and gluconeogenesis.
• Insulin promotes the transport and incorporation of amino acids into
cells for protein synthesis.

59. Fig. 17-25, p. 566
Gastrointestinal
hormones
Blood glucose
concentration
Blood amino acid
concentration
Major control
Food
intake
Parasympathetic
stimulation
Islet  cells
Sympathetic stimulation
(and epinephrine)
Insulin secretion
Blood glucose
Blood fatty acids
Blood amino acids
Protein synthesis
Fuel storage

60. Fig. 17-27, p. 572
Blood glucose
 cell  cell
Glucagon Insulin
Blood glucose
to normal
Blood glucose
 cell  cell
Glucagon Insulin
Blood glucose
to normal

61. Table 17-7, p. 572

62. An increase in blood glucose
concentration increases the secretion
of insulin.
• This secretion (e.g., during the absorptive state) brings blood
glucose down to a normal level.
• A fall in glucose below normal inhibits insulin secretion. This shifts
metabolism from the absorption to the postabsorptive pattern.
• Elevated amino acids in the blood stimulate insulin secretion. The
sympathetic nervous system decreases insulin secretion.
• Inadequate insulin action produces diabetes mellitus. The result is
hyperglycemia. Type I diabetes mellitus is due to an insulin
deficiency. Type II is due to the reduced sensitivity of target cells to
the presence of the hormone.

63. Low insulin activity has several
consequences.
• Except for hyperglycemia the effect is similar to a prolonged
postabsorptive state on carbohydrate metabolism.
• Glucosuria occurs. Excess urination also occurs. This can lead to
circulatory failure, renal failure, and dehydration.
• Lipolysis is decreased. Fatty acids are mobilized from triglycerides.
Liver use of fatty acids leads to ketosis. Acidosis develops and can
depress brain function.
• Protein metabolism shifts to protein catabolism. This can reduce
growth and lead to the wasting of skeletal muscles.
• Long-term complications of diabetes mellitus include degenerative
disorders of the vascular and nervous systems.

64. Diabetes Mellitus
• The major features of DM are:
1.Hyperglycemia (increased blood glucose levels)
is the corner stone presentation in DM.
2.Polyuria – increased urine output
3.Polydipsia – excessive thirst
4.Polyphagia – excessive hunger and food
consumption

65. p. 569

66. Fig. 17-26, p. 570
Insulin deficiency
Hepatic
glucose
output
Glucose
uptake
by cells
Triglyceride
synthesis
Lipolysis
Amino acid
uptake by cells
Protein
degradation
Hyperglycemia Intracellular
glucose
deficiency
Blood
fatty
acids
Muscle
wasting
Glucosuria
Polyphagia
Alternative
energy source
Blood
amino
acids
Weight
loss
Osmotic diuresis
Polyuria
Dehydration Polydipsia Ketosis
Gluconeogenesis
Cellular
shrinking
Blood volume
Peripheral
circulatory
failure
Renal failure
Death
Low cerebral
blood flow
Nervous system
malfunction
Metabolic
acidosis
Diabetic
coma
Increased
ventilation
Aggravation of
hyperglycemia

67. Other facts on blood glucose control include:
• Insulin excess causes brain-starving hypoglycemia. The brain
cannot store glycogen and starves under this circumstance.
• Glucagon opposes the actions of insulin. It promotes
glycogenolysis. This hormone also promotes fat breakdown. In
addition, it promotes the breakdown of proteins in the liver.
• Glucagon secretion increases during the postabsorptive state. Its
secretion increases when the blood concentration of glucose is too
low.
• Therefore, insulin and glucagon work as a team to control the
concentration of glucose and fatty acids in the blood.
• However, an excess of glucagon can aggravate the hyperglycemia
of diabetes mellitus.
• The growth hormone, cortisol, epinephrine, and glucagon are
insulin antagonists. They increase blood glucose.